PMID- 8945953
OWN - NLM
STAT- MEDLINE
DCOM- 19970103
LR  - 20171213
IS  - 0002-9513 (Print)
IS  - 0002-9513 (Linking)
VI  - 271
IP  - 5 Pt 2
DP  - 1996 Nov
TI  - Endogenous modulators of TNF and IL-1 response are under partial control of TNF 
      in baboon bacteremia.
PG  - R1193-8
AB  - Tumor necrosis factor (TNF) and interleukin (IL)-1 are two cytokines for which 
      naturally occurring inhibitors have been identified. The present study was 
      undertaken to evaluate the extent to which scavenging of TNF in bacteremia 
      attenuates the plasma levels of IL-1 receptor antagonist (IL-1ra) and soluble TNF 
      receptors (sTNFR). Ten male baboons received 2 x 10(9) colony-forming units/kg 
      live Escherichia coli over 2 h and were subjected to either placebo or anti-TNF 
      antibody (anti-TNF Ab) treatment (1 mg/kg CDP571, Celltech, UK) 2 h before E. 
      coli infusion (observation time: 72h). IL-1ra (range: 50-100 ng/ml) and sTNFR 
      (range: 55kDa, 20-25 ng/ml; 75 kDa, 30-35 ng/ml) release was more sustained than 
      that of IL-1 and TNF and was significantly attenuated by anti-TNF treatment, as 
      were the circulating levels of IL-1, IL-8, and monocyte chemotactic peptide-1 
      (MCP-1) in the anti-TNF Ab group. We conclude that the increase in circulating 
      natural cytokine modulators observed in nonhuman primate bacteremia is under the 
      partial control of endogenous TNF because it was influenced by anti-TNF 
      pretreatment. This attenuation is comparable to the anti-TNF effect on the 
      chemokine MCP-1.
FAU - Redl, H
AU  - Redl H
AD  - Ludwig Boltzmann Institute for Experimental and Clinical Traumatology, Vienna, 
      Austria.
FAU - Schlag, G
AU  - Schlag G
FAU - Paul, E
AU  - Paul E
FAU - Bahrami, S
AU  - Bahrami S
FAU - Buurman, W A
AU  - Buurman WA
FAU - Strieter, R M
AU  - Strieter RM
FAU - Kunkel, S L
AU  - Kunkel SL
FAU - Davies, J
AU  - Davies J
FAU - Foulkes, R
AU  - Foulkes R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Am J Physiol
JT  - The American journal of physiology
JID - 0370511
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-1)
RN  - 0 (Interleukin-8)
RN  - 0 (Receptors, Interleukin-1)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Antibodies, Monoclonal/immunology
MH  - Bacteremia/blood/*physiopathology
MH  - Chemokine CCL2/blood
MH  - *Escherichia coli Infections
MH  - Interleukin-1/*blood
MH  - Interleukin-8/blood
MH  - Male
MH  - Papio
MH  - Receptors, Interleukin-1/antagonists & inhibitors
MH  - Receptors, Tumor Necrosis Factor/blood
MH  - Solubility
MH  - Tumor Necrosis Factor-alpha/immunology/*metabolism/*physiology
EDAT- 1996/11/01 00:00
MHDA- 1996/11/01 00:01
CRDT- 1996/11/01 00:00
PHST- 1996/11/01 00:00 [pubmed]
PHST- 1996/11/01 00:01 [medline]
PHST- 1996/11/01 00:00 [entrez]
AID - 10.1152/ajpregu.1996.271.5.R1193 [doi]
PST - ppublish
SO  - Am J Physiol. 1996 Nov;271(5 Pt 2):R1193-8. doi: 
      10.1152/ajpregu.1996.271.5.R1193.